Description:

Epidemiological studies demonstrate an association between increased levels of ambient air pollution particles and human morbidity and mortality. Production of oxidants, either directly by the air pollution particles or by the host response to the particles, appears to be fundamental in the biological effect after exposure to particulate matter (PM). However, the precise components and mechanisms responsible for oxidative stress following PM exposure are yet to be defined. Direct oxidant generation by air pollution particles is attributed to organic and metal components. Organic compounds generate an oxidative stress through redox cycling of quinonebased radicals, by complexing of metal resulting in electron transport, and by depletion of antioxidants
by reactions between quinones and thiol-containing compounds. Metals can directly support electron transport to generate oxidants and can also diminish levels of anti-oxidants. In addition to direct generation of oxidants by organic and metal components, cellular responses contribute to oxidative stress after PM exposure. Reactive oxygen species production occurs in the mitochondria, cell membranes, phagosomes, and the endoplasmic reticulum. Oxidative stress following PM exposure initiates a series of cellular reactions that includes activation of kinase cascades and transcription factors, release of inflammatory mediators, which can ultimately lead to cell injury or apoptosis. Consequently, oxidative stress in cells and tissues is a central mechanism by which PM exposure leads to injury, disease, and mortality.
oxide

Purpose/Objective:

Production of oxidants, either directly by the air pollution particles or by the host response to the particles, appears to be fundamental in the biological effect after exposure to particulate matter (PM).